BIOCHEMICAL MODELS OF HETEROSIS IN NEUROSPORA 213 



for allelism are available. The inference that they are distinct genes is based 

 on the data summarized in Table 12.2. 



The reactions controlled by the suppressor genes have not been identified. 

 Suppressor SA is stimulated in growth by additional /)-aminobenzoic acid, 

 and is inhibited considerably by sulfanilamide at concentrations twenty 

 times less than that required to inhibit wild type. It is possible that a de- 

 ficient amount of />-aminobenzoic acid is produced by this mutant, which 

 would make it approximate the condition in one of the model heterocaryons. 

 Growth of suppressor S-2 is somewhat stimulated by sulfanilamide (Fig. 

 12.4) and by threonine, in this respect resembling the sulfonamide-requiring 

 mutant which it "suppresses." It is even more stimulated by the purine, 



TABLE 12.2 



EVIDENCE SUGGESTING THAT SUP- 

 PRESSORS 5i, S2, Si, AND Se ARE 

 DIFFERENT GENES 



adenine, as shown by the growth curves in Figure 12.7. It was previously 

 known that in the presence of methionine, adenine reduces the normal re- 

 quirement for />-aminobenzoic acid to about one-tenth its usual value. This 

 suggested that the production of adenine also requires /)-aminobenzoic acid. 

 The reaction controlled by this suppressor may thus be closely related to 

 that controlled by the sulfonamide-requiring gene. No clues have turned up 

 to indicate how the reactions governed by the remaining suppressor muta- 

 tions may be related to these. 



In the living cell of Neurospora the reactions which are influenced in one 

 way or another by the amount of available /»-aminobenzoic acid must be fairly 

 numerous. The production of adenine and methionine requires the presence 

 of this vitamin as does the reaction in the sulfonamide-requiring mutant 

 which makes threonine unavailable. 



Strauss (1950) has studied a mutant strain (44602) which requires pyri- 

 do.xine unless grown at high pH with ammonia as nitrogen source. He found 

 that under the latter conditions it is inhibited by methionine, and that this 

 inhibition is reversed by sulfanilamide, as if />-aminobenzoic acid were re- 

 quired for the inhibition. Still another interrelationship has been found by 

 Shen (1950) in studies of a mutant strain (84605) which requires sulfur in a 



